title: The impact of metabolic syndrome on insulin sensitivity, glucose sensitivity, and acute insulin response after glucose load in early-onset type 2 diabetes mellitus: Taiwan Early-Onset Type 2 Diabetes Cohort Study.
abstract: Diabetic patients with metabolic syndrome (MetS) have higher lifetime risks for cardiovascular disease, especially in early-onset type 2 diabetes mellitus (EODM). Increased insulin resistance (IR) and impaired insulin secretion are important pathophysiologies in diabetic patients. Therefore, the effects of MetS on IR and insulin secretion in EODM were investigated. Forty-eight EODM (mean age, 22.8 +/- 0.6 years) patients were enrolled in this study. Two grouping criteria were used: the first was whether the patient had MetS or not (MetS+ or Met-, with 31 and 17 patients, respectively); and the second was the number of MetS components each group had, that is, MetS (1,2) with 1 to 2, MetS (3) with 3, and MetS (4,5) with 4 to 5 components (17, 17, and 14 patients in each group, respectively). A frequently sampled intravenous glucose tolerance test was performed to measure insulin sensitivity, glucose sensitivity, acute insulin response after glucose load, and disposal index. Severe IR was noted with both homeostasis model assessment and frequently sampled intravenous glucose tolerance test both in MetS+ and MetS-. However, significantly higher acute insulin response after glucose load and disposal index were noted in MetS+ and MetS (4,5) than in Met-, MetS (1,2), and MetS (3), respectively. Early-onset type 2 diabetes mellitus patients with MetS had similar IR to those without MetS. This may be due to early deterioration of insulin action in these subjects. In addition, insulin secretion was higher in subjects with more MetS components, suggesting that EODM patients with MetS had better preserved ability of beta-cell compensation for IR than those without MetS.
authors.affiliation: Division of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, Taipei, Taiwan, ROC.
authors.forename: Chang-Hsun
authors.initials: CH
authors.lastname: Hsieh
authors.forename: Chung-Ze
authors.initials: CZ
authors.lastname: Wu
authors.forename: Fone-Ching
authors.initials: FC
authors.lastname: Hsiao
authors.forename: Jiunn-Diann
authors.initials: JD
authors.lastname: Lin
authors.forename: Jer-Chuan
authors.initials: JC
authors.lastname: Li
authors.forename: Hsiang-Lin
authors.initials: HL
authors.lastname: Wan
authors.forename: Shi-Wen
authors.initials: SW
authors.lastname: Kuo
authors.forename: Yi-Jen
authors.initials: YJ
authors.lastname: Hung
authors.forename: Ching-Chieh
authors.initials: CC
authors.lastname: Su
authors.forename: Dee
authors.initials: D
authors.lastname: Pei
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D015331:Cohort Studies; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism*; D005260:Female; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000502:physiology; D008297:Male; D024821:Metabolic Syndrome / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D007328:Insulin